Theorists agree that living
organisms possess extensive maintenance and repair functions that act to repair
damage. This is a major and obvious difference between living organisms and
non-living entities and a main reason that the generic wear
and tear theories do not work. As a result, there now exist both programmed
and non-programmed theories of aging based on maintenance and repair functions.

Maintenance and Repair
Functions

Here are examples of known
maintenance and repair functions:

Claws, nails, hair, and fur grow
to replace worn items.

Wounds heal.

Dead cells are replaced. Some
cells (e.g. epithelial cells) only last a short time (weeks).

According to traditional
evolutionary mechanics theory, an organism cannot evolve a mechanism whose
primary purpose is to limit life span but can evolve maintenance mechanisms whose purpose is
to extend life span. Because of
Medawar's hypothesis, organisms do not need life spans longer than some
multiple of their age of sexual maturity and therefore there is little or no
evolutionary motivation towards developing and retaining maintenance mechanisms capable of
delaying deterioration beyond that point.

Different manifestations of aging
appear to be caused by greatly different mechanisms. Much heart disease is
caused by buildup of artery deposits. Cancer appears to be caused by molecular
changes that cause uncontrolled cell growth. These mechanisms are very different
leading to the conclusion that different maintenance and repair mechanisms are
involved in repair of damage leading to various different manifestations.
This leads to the idea that a number (potentially a large number) of different
maintenance mechanisms evolved independently. If an animal species was troubled
by excessively early heart disease it would evolve better anti-heart disease
mechanisms. If cancer became a problem, it would evolve a better anti-cancer mechanism and so
forth. Non-programmed maintenance theories suggest that in each species, the
various maintenance mechanisms have each been tailored by the evolution process to that species' need for
life span. In a short-lived species, all of the maintenance functions are
somehow less effective and therefore unrepaired damage accumulates more rapidly
than in a longer-lived species.

According to alternative evolutionary mechanics theories and
associated aging theories, an
organism can evolve both anti-aging functions necessary to achieve a life span
loosely based on Medawar's criteria, and a life span regulation
mechanism necessary to limit life span to a species-specific
value also loosely based on Medawar's criteria. A life span exceeding the
optimum life span for the species creates evolutionary disadvantage.
Therefore, assuming the same sorts of maintenance functions described above,
the combined system could be as described below. In this concept a biological
life span regulation function purposely discontinues or slows maintenance
functions at a species-unique age. Like most evolved biological functions, the
proposed regulation mechanism is capable of adapting (within a genetically designed range) to local or
temporary conditions via sense functions. In this concept the major difference
between mammal species is in the control (clock, sense, signaling) mechanism
as opposed to differences in each of the maintenance mechanisms.

A major feature of
this concept is the existence of mechanisms that are common to
multiple manifestations of aging including clock, sensory, and signaling
functions. This contrasts with the non-programmed concept of independent
maintenance functions and has major medical
implications.

Progeria and Werner Syndrome: These human conditions
accelerate many or most manifestations of aging. That a single-gene
malfunction affects multiple manifestations suggests commonality between
causes, which fits programmed theory but not independent maintenance
mechanisms.

Caloric Restriction and Stress Response: Programmed
theories suggest that there would be benefit to a life span regulation
mechanism that responded to these temporary conditions by adjusting life span.
The suggested programmed mechanism matches observations. These observations
are essentially incompatible with the non-programmed theory.

Common Aging Manifestations: Even though there is a
100:1 range in mammal life spans,
manifestations of aging are remarkably similar between mammal species. It
seems implausible that this would be the case in the non-programmed scenario.

Short-term Nature of Maintenance: The example
maintenance functions are short-term and operate over periods of weeks or
months. The maintenance necessary for all of the major manifestations of aging
is also short-term. If it was not, short-lived animals would not display some
of the manifestations. This is a difficulty for the non-programmed theory: Why
would a function that successfully held off cancer between mouse age and cat age
in the cat fail to achieve human life span in the cat?

Rapid Adaptation: If one assumes that a
species-specific design-limited life span has merit then the life span
regulation mechanism concept is clearly superior in that it can adjust rapidly
to a species' adaptive need for shorter or longer life span. All of the
maintenance functions can be adjusted by altering a few genes or even single
gene associated with the control mechanism.

Aging Genes: The finding that a single gene can
significantly affect life span suggests commonality.

Digital Genetics: The digital nature of genetics data
imposes limits on the degree of variability possible in any parameter. In a
digital system nothing is indefinitely variable. This makes it difficult to
imagine the sort of continuous variation in maintenance mechanisms necessary to explain multi-species
observations in the non-programmed case. Would we need a 99 percent effective
anti-cancer mechanism in rats, a 99.9 percent effective mechanism in cats,
perhaps 99.99 percent effective in humans and what, 99.9999 percent in
negligibly senescent species? How would each of the maintenance mechanisms actually differ
from species to species in order
to produce the observed effects? This is not a problem for the programmed
mechanism.